Asbestos Fibers and Other Elongate Mineral Particles: State of the ...

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to crocidolite fibers and TNF-α caused greater damage than fibers alone. Antioxidant enzymes did not reduce the DNA damage, suggesting a mechanism of damage other than by free radicals [Ollikainen et al. 1999]. Crocidolite fibers were also very cytotoxic to the cells; presumably, cell death may prevent the observation of cell transformation. In vitro challenge to mesothelial cells and to fibroblast cells by crocidolite fibers, but not by glass wool, induced dose-dependent cytotoxicity and increased DNA synthesis activity [Cardinali et al. 2006]. Crocidolite fibers were found to induce TNF-α secretion and receptors in human mesothelial cells, and TNF-α reduced cytotoxicity of crocidolite fibers by activating NF-κB and thus improving cell survival and permitting expression of cytogenetic activity [Yang et al. 2006]. Erionite fibers transformed immortalized nontumorigenic human mesothelial cells in vitro only when exposed in combination with IL-1β or TNF-α [Wang et al. 2004]. Erionite fibers were poorly cytotoxic but induced proliferation signals and a high growth rate in hamster mesothelial cells. Long-term exposure to erionite fibers resulted in transformation of human mesothelial cells in vitro, but exposure to asbestos fibers did not transform those cells [Bertino et al. 2007]. In vitro challenge of mesothelial cells to asbestos fibers induced cytotoxicity and apoptosis but not transformation. In vitro challenge of human mesothelial cells to asbestos fibers induced the ferritin heavy chain of iron-binding protein, an anti-apoptotic protein, with decrease in H 2O 2 and other ROS and resistance to apoptosis [Aung et al. 2007]. This was seen also in a human malignant mesothelial cell line. The question of a co-carcinogenic effect of asbestos fibers with a virus has been raised. Most malignant mesotheliomas are associated with asbestos exposures, but only a fraction of exposed individuals develop mesothelioma, indicating that other factors may play a role. It has 54 been suggested that simian virus 40 (SV40) and asbestos fibers may be co-carcinogens. SV40 is a DNA tumor virus that causes mesothelioma in hamsters and has been detected in several human mesotheliomas. Asbestos fibers appear to increase SV40-mediated transformation of human mesothelial cells in vitro [Carbone et al. 2002]. In an in vivo demonstration of co-carcinogenicity of SV40 and asbestos fibers, mice containing high copy numbers of SV40 viral oncogene rapidly developed fast-growing mesothelioma following asbestos challenge. Transgenic copy number was proportional to cell survival and in vitro proliferation [Robinson et al. 2006]. Various mechanisms protect cells and tissues against oxidants, and it is conceivable that genetic and acquired variations in these systems may account for individual variation in the response to oxidative stress [Driscoll et al. 2002]. Similarly, species differences in antioxidant defenses or the capacity of various defenses may underlie differences in response to xenobiotics that act, in whole or part, through oxidative mechanisms. Oxidative mechanisms of response to xenobiotics are especially relevant to the respiratory tract, which is directly and continually exposed to an external environment containing oxidant pollutants (e.g., ozone, oxides of nitrogen) and particles that may generate oxidants as a result of chemical properties or by stimulating production of cell-derived oxidants. In addition, exposure to particles or other pollutants may produce oxidative stress in the lung by stimulating the recruitment of inflammatory cells. For example, the toxicity of asbestos fibers likely involves the production of oxidants, such as hydroxyl radical, SO, and H 2O 2. Studies have also shown that asbestos fibers and other mineral particles may act by stimulating cellular production of ROS and reactive nitrogen species. In addition to NIOSH CIB 62 • Asbestos
direct oxidant production, exposure to asbestos and SVFs used in high-dose animal studies stimulates the recruitment and activation of macrophages and polymorphonuclear leukocytes that can produce ROS through the activity of NADPH oxidase on their cell membranes. Developing an understanding of the oxidative stress/NF-ĸB pathway for EMP-mediated inflammation and the interplay among exposureinduced oxidant production, host antioxidant defenses, and interindividual or species variability in defenses may be very important for appropriate risk assessments of inhaled EMPs [Donaldson and Tran 2002]. 2.9.4.4 Studies Comparing EMPs from Amphiboles with Asbestiform versus Nonasbestiform Habits Smith et al. [1979] compared tumor induction after IP injection in hamsters of two asbestiform tremolites, two nonasbestiform prismatic tremo litic talcs, and one tremolitic talc of uncertain asbestiform status. No tumors were observed following the nonasbestiform tremolite challenge, in contrast to the asbestiform tremo lites. However, tumors were observed from the tremolitic talc of uncertain amphibole status. In rule-making, OSHA [1992] noted the small number of animals in the study, the early death of many animals, and the lack of systematic characterization of particle size and aspect ratio. Subsequent analyses (by chemical composition) performed on the nonasbestiform tremolitic talc from the study, which was not associated with mesothelioma, found 13% of particles had at least a 3:1 aspect ratio [Wylie et al. 1993]. A prismatic, nonasbestiform tremolitic talc and an asbestiform tremolite from the study were analyzed for aspect ratio [Campbell et al. 1979]. The researchers analyzed 200 particles of the asbestiform tremolite sample and found 17% had an aspect ratio of 3:1 or greater and 9.5% NIOSH CIB 62 • Asbestos had an aspect ratio greater than 10:1. Analysis of 200 particles of the prismatic tremolite showed that 2.5% (five EMPs) had an aspect ratio of 3:1 or greater and 0.5% (one EMP) had an aspect ratio greater than 10:1. Wagner et al. [1982] challenged rats by IP injection of tremolite asbestos, a prismatic nonasbestiform tremolite, or a tremolitic talc considered nonasbestiform containing a limited number of long fibers. Only the tremolite asbestos produced tumors; mesothelioma was found in 14 of 37 animals. The authors speculated that tumor rate may have risen further if the testing period had not been shortened due to infectioninduced mortality. Per microgram of injected dose, the asbestiform sample contained 3.3 × 10 4 nonfibrous particles, 15.5 × 10 4 fibers, and 56.1 × 10 3 fibers >8 µm long and 3:1 per 121 × 106 fibers with length >8 µm and diameter
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CURRENT INTELLIGENCE BULLETIN 62 As
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CURRENT INTELLIGENCE BULLETIN 62 As
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Foreword Asbestos has been a highly
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Executive Summary In the 1970s, NIO
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NIOSH recognizes that its 1990 desc
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of exposure to various types of EMP
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xii 2.9.3 Biopersistence and other
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xiv List of Figures Figure 1. U.S.
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xvi MAPK mitogen-activated protein
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xviii Brooke Mossman, PhD Universit
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controlled, even when exhaustive lo
Page 25 and 26: 2 Overview of Current Issues 2.1 Ba
Page 27 and 28: juxtaposition or matrixed together,
Page 29 and 30: A further source of confusion comes
Page 31 and 32: Figure 2. Asbestos: Annual geometri
Page 33 and 34: Figure 3. Number of asbestosis deat
Page 35 and 36: at home by playing in areas where a
Page 37 and 38: physician from an occupational and
Page 39 and 40: of airborne asbestos fibers was fir
Page 41 and 42: which the deposits have been report
Page 43 and 44: with the most pronounced excess of
Page 45 and 46: A limitation of the epidemiological
Page 47 and 48: CI = 1.8-6.7) was noted in the earl
Page 49 and 50: exposure to commercial asbestos, an
Page 51 and 52: of these populations should be purs
Page 53 and 54: affect only a small number of obser
Page 55 and 56: exposed to fibers considerably long
Page 57 and 58: the extent to which the material ha
Page 59 and 60: or statistical power to permit a co
Page 61 and 62: capillaries, whereas insoluble part
Page 63 and 64: mechanisms and increase the rate of
Page 65 and 66: can penetrate their interior to pro
Page 67 and 68: A review for the EPA by an internat
Page 69 and 70: 2.9.4.3.1 Reactive Oxygen Species A
Page 71 and 72: of different types of mineral parti
Page 73: secreted by mesothelial cells after
Page 77 and 78: widths are greater for the prismati
Page 79 and 80: concluded that asbestos fibers
Page 81 and 82: crystal structure, and surface comp
Page 83 and 84: is calibrated appropriately for NIO
Page 85 and 86: is made of an area larger than a si
Page 87: data are needed to more fully asses
Page 90 and 91: 70 III. Develop improved sampling a
Page 92 and 93: the current paradigm because their
Page 94 and 95: on the development of disease endpo
Page 96 and 97: esponse, and time-course data would
Page 98 and 99: In the second phase of cellular res
Page 100 and 101: 80 • Investigate mechanisms of EM
Page 102 and 103: Research is needed to produce infor
Page 104 and 105: periods that characterize manifesta
Page 106 and 107: children in tow, placing both sexes
Page 108 and 109: 88 • Develop, validate, and promo
Page 110 and 111: elevant, then an exposure assessmen
Page 112 and 113: ased on counts made by the current
Page 114 and 115: established precedence in applying
Page 116 and 117: the mechanisms by which asbestos fi
Page 119 and 120: 4 The Path Forward Developing an in
Page 121 and 122: surveillance investigations. By hav
Page 123 and 124: 5 References Aadchi S, Yoshida S, K
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Berman DW, Crump KS [2008b]. A meta
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mineral fiber number and epidemiolo
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the United States, 1968-81. J Natl
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Greim HA [2004]. Research needs to
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France: International Agency for Re
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millers in New York State. Arch Env
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Mandel J (mand0125@umn.edu) [2008].
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gpo.gov/2008/pdf/E8-3828.pdf]. Date
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Pneumoconioses to Digital Chest Rad
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Potter RM [2000]. Method for determ
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glass: pleural response in the rat
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Vianna NJ, Maslowsky J, Robert S, S
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Yano E, Wang Z, Wang X [2001]. Canc
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efficiency, regardless of sampler o
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Table 1. Definitions of general min
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Table 2. Definitions of specific mi
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safer • healthier • people tm D
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